2019
Mitochondrial DNA stress signalling protects the nuclear genome
Wu Z, Oeck S, West AP, Mangalhara KC, Sainz AG, Newman LE, Zhang XO, Wu L, Yan Q, Bosenberg M, Liu Y, Sulkowski PL, Tripple V, Kaech SM, Glazer PM, Shadel GS. Mitochondrial DNA stress signalling protects the nuclear genome. Nature Metabolism 2019, 1: 1209-1218. PMID: 32395698, PMCID: PMC7213273, DOI: 10.1038/s42255-019-0150-8.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Line, TumorCell NucleusCytosolDNA DamageDNA, MitochondrialDNA-Binding ProteinsGenomeHigh Mobility Group ProteinsInterferonsInterferon-Stimulated Gene Factor 3Membrane ProteinsMiceMice, KnockoutMice, NudeNF-kappa BNucleotidyltransferasesProtein Serine-Threonine KinasesSignal TransductionConceptsMtDNA stressNuclear DNAGene expressionThousands of copiesMost cell typesRepair responseAcute antiviral responseNuclear genomeCircular mtDNAHigher-order structureInterferon gene expressionEssential proteinsMitochondrial DNACultured primary fibroblastsDNA stressUnphosphorylated formInterferon-stimulated gene expressionMouse melanoma cellsNDNA repairSignaling responseOxidative phosphorylationNDNA damageMtDNA damageMtDNAPrimary fibroblasts
2001
Chromosome Targeting at Short Polypurine Sites by Cationic Triplex-forming Oligonucleotides*
Vasquez K, Dagle J, Weeks D, Glazer P. Chromosome Targeting at Short Polypurine Sites by Cationic Triplex-forming Oligonucleotides*. Journal Of Biological Chemistry 2001, 276: 38536-38541. PMID: 11504712, DOI: 10.1074/jbc.m101797200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceCationsChromosomesCOS CellsDiaminesDNADNA Mutational AnalysisDose-Response Relationship, DrugEthylenediaminesFicusinGenes, ReporterGenes, SuppressorGenetic TechniquesGenomeIndicators and ReagentsMagnesiumMiceMice, KnockoutModels, GeneticMolecular Sequence DataMutagenesisMutagenesis, Site-DirectedNucleic Acid ConformationPotassiumProtein BindingPurinesRNA, TransferSequence Homology, Nucleic AcidConceptsChromosomal reporter geneMonkey COS cellsTarget siteSite-specific mutationsTriplex target sitesChromosome targetingEpisomal targetChromosomal targetsGene mutagenesisMammalian cellsSite-specific inductionChromosomal lociReporter geneCOS cellsGene knockoutGenomic DNAMouse cellsSite-directed modificationOligonucleotide bindsPhosphodiester bondShort sitesThird strand bindingPhosphodiester backboneSystemic administrationDNAHypermutability to ionizing radiation in mismatch repair-deficient, Pms2 knockout mice.
Xu X, Narayanan L, Dunklee B, Liskay R, Glazer P. Hypermutability to ionizing radiation in mismatch repair-deficient, Pms2 knockout mice. Cancer Research 2001, 61: 3775-80. PMID: 11325851.Peer-Reviewed Original ResearchConceptsMismatch repairSimple sequence repeatsWild-type transgenic miceCell linesLambda cII geneMutation frequencyDNA mismatch repairHigher clonogenic survivalMMR-deficient miceLambda shuttle vectorTolerance phenotypeSequence repeatsPatterns of IRReporter geneRepeat sequencesMononucleotide repeat sequencesShuttle vectorSingle bp deletionCII geneNullizygous animalsNullizygous miceHypermutabilityBp deletionWild-type miceClonogenic survival
2000
Ionizing radiation-induced apoptosis via separate Pms2- and p53-dependent pathways.
Zeng M, Narayanan L, Xu X, Prolla T, Liskay R, Glazer P. Ionizing radiation-induced apoptosis via separate Pms2- and p53-dependent pathways. Cancer Research 2000, 60: 4889-93. PMID: 10987303.Peer-Reviewed Original ResearchMutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts
Andrew S, Xu X, Baross-Francis A, Narayanan L, Milhausen K, Liskay R, Jirik F, Glazer P. Mutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts. Carcinogenesis 2000, 21: 1291-1296. PMID: 10874005, DOI: 10.1093/carcin/21.7.1291.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphatasesAnimalsBase Pair MismatchCrosses, GeneticDNA RepairDNA Repair EnzymesDNA-Binding ProteinsFemaleFrameshift MutationGenes, ReporterGenotypeGerm-Line MutationMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicMismatch Repair Endonuclease PMS2MutagenesisMutS Homolog 2 ProteinPoint MutationProteinsProto-Oncogene ProteinsConceptsPms2-deficient miceMsh2-deficient miceHereditary non-polyposis colorectal cancer patientsCII target geneDNA mismatch repair deficiencyColorectal cancer patientsPMS2 germline mutationsMismatch repair deficiencyReporter transgenic miceMutation frequencyLacI target geneCancer patientsTarget genesMouse modelKnockout miceTumor spectrumTransgenic miceFrameshift mutationGermline mutationsMiceRepair deficiencyPMS2 deficiencySupF target geneMSH2Predominant mutations
1999
Different mutator phenotypes in Mlh1- versus Pms2-deficient mice
Yao X, Buermeyer A, Narayanan L, Tran D, Baker S, Prolla T, Glazer P, Liskay R, Arnheim N. Different mutator phenotypes in Mlh1- versus Pms2-deficient mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 1999, 96: 6850-6855. PMID: 10359802, PMCID: PMC22005, DOI: 10.1073/pnas.96.12.6850.Peer-Reviewed Original ResearchConceptsMismatch repairMutator phenotypeMutation rateDifferent chromosomal locationsSingle-molecule PCRDinucleotide repeat lociMutation frequencyDNA mismatch repairMononucleotide repeat tractsChromosomal locationCellular processesDNA repair capacityHigh mutation frequencyDifferent mutator phenotypesMultiple genetic alterationsKnockout strainRepeat tractMlh1pMLH1 MMR geneRepeat lociGenetic alterationsDifferent tumor spectrumRepair capacityTumor developmentMMR genes